10 results about "Caspase 3" patented technology

Abstract Described herein, in one aspect, are antigen presenting cells (APCs) comprising an exogenous nucleic acid encoding one or more candidate antigens, wherein the one or more candidate antigens are expressed and presented with MHC class I or MC class II molecules; a molecular reporter of Granzyme B (GzB) activity; and c) an exogenous inhibitor of caspase-activated deoxyribonuclease (CAD)-mediated DNA degradation, a CAD knockout, or a caspase knockout (e.g., caspase 3 knockout). Described herein, in another aspect, is a system for detection of recognized antigen presentation by an antigen presenting cell to a cytotoxic lymphocyte or NK cell. Abstract 2018 / 22761 oM - cell Target ml Target cell cell cell Target Target Target SUBSTITUTE SHEET (RULE 26) cell cell cell Target Target cell cell 1 / 28 my Isolate recognized cell Library of target cells target cells and displaying different Add T cells from sample sequence antigens antigens of interest. CTLs deliver cytotoxic granules to target cells displaying cognate antigen FIG. 1 PCT / US2018 / 036663 20 26 20 53 56 07 J ul 2 02 6 2 0 2 6 2 0 5 3 5 6 0 7 J u l 2 0 2 6 2 0 1 8 / 2 2 7 6 1 o M a n d m y 1 / 2 8 m y L i b r a r y o f t a r g e t c e l l s d i s p l a y i n g d i f f e r e n tA d d T c e l l s f r o m s a m p l e of interest. CTLs deliver c y t o t o x i c g r a n u l e s t o t a r g e t c e l l s d i s p l a y i n g c o g n a t e a n t i g e n P C T / U S 2 0 1 8 / 0 3 6 6 6 3

The invention provides an application of an epidermal growth factor (EGF) in induction of apoptosis of an upper urinary tract epithelial carcinoma organ (UTUC), and belongs to the technical field of biomedicine. The invention relates to an application of an EGF (Epidermal Growth Factor) or EGFR (Epidermal Growth Factor Receptor) agonist in inducing The EGF induces apoptosis of the upper urinary tract epithelial cancer organoid by activating the STAT1-Caspase 3 pathway and up-regulating the expression level of the EGFR. In view of the fact that the upper urinary tract epithelium carcinoma organoid and the upper urinary tract epithelium carcinoma tissue are highly consistent in form and regulation mechanism, the technical scheme provided by the invention provides a new thought for the medicine for preventing and / or treating the upper urinary tract epithelium carcinoma.

The present disclosure relates generally to alkyne containing pharmaceutical agents, and in particular, to phenylethynyl-thiophene based compounds. More particularly, the present disclosure provides a class of compounds that can inhibit and / or attenuate apoptosis via caspase 3 for the treatment of various degenerative disorders. Additionally, the present disclosure relates to methods for treating specific degenerative disorders such as amyotrophic lateral sclerosis (ALS), Huntington's disease, epilepsy, spinal cord injury, complication due to diabetes, multiple sclerosis (MS), muscular dystrophy (MD), Parkinson's disease (PD), irritable bowel syndrome (IBS) and Alzheimer's disease (AD) in a patient comprising administering to the patient an effective amount of a present compound.

The invention provides for a screening assay-using a selective proteolysis of recombinant full-length PIKfyve at an endogenous caspase 3 cleavage site to liberate the 34 kDa C -terminal kinase domain. Despite instability of the kinase domain to isolation, the liberated kinase domain is stable in the presence of the N-terminal PIKfyve protein fragment and can thus be treated with compounds of interest and analyzed by mass spectrometry, such as RapidFire-MS, with each injection taking under one minute. The assay was established to triage small molecules for covalent modification of PIKfyve. The assay was also established using cysteine-mutant proteins, where the reactive cysteine was replaced with an inert amino acid which when run through the same experimental protocol, was used to confirm adduct formation at the target cysteine.

The invention relates to application of liquiritigenin in preparation of a medicine for relieving muscle injury caused by exercise fatigue, in particular to application of liquiritigenin in preparation of a medicine for relieving muscle injury caused by exercise fatigue, specifically, liquiritigenin inhibits expression of Caspase 3 by up-regulating the proportion of PI3K / Akt protein so as to inhibit muscle cell apoptosis; meanwhile, liquiritigenin reduces expression of inflammatory factors by up-regulating the proportion of PI3K / Akt protein, so that muscle injury caused by exercise fatigue is relieved; specifically, the liquiritigenin can further prolong the exhaustive exercise time of the mouse, enhance the endurance and improve the exercise ability of the mouse on the basis of improving the endurance of the mouse.

The invention discloses a composite probiotic fermentation method and application, and belongs to the technical field of fermentation. Saccharomyces cerevisiae and kluyveromyces marxianus are used as compound probiotics for fermentation to prepare a compound yeast culture, the compound yeast culture and a plant extract form a compound, and the compound shows a synergistic interaction effect, specifically, the rumen papillary protrusion length and the rumen surface area are increased, the cell cycle progress is accelerated, and the effect of improving the rumen papillary protrusion length and the rumen surface area is achieved. Compared with the prior art, the rumen epithelial cell culture medium has the advantages that the density of living cells is higher, rumen epithelial cell proliferation is promoted, the expression of apoptosis related genes caspase 3, Cyt-c, Fas and TNFR1 is remarkably reduced, and the apoptosis of rumen epithelial cells is relieved. The method not only has practical value for comprehensive utilization of the compound yeast culture obtained by fermentation of the compound probiotics, but also has important value for promoting ruminant rumen epithelium development.

The application discloses application of norisoboldine or a pharmaceutically acceptable salt, a polymorph or a solvate thereof in preparation of a drug for preventing or treating myocardial ischemia-reperfusion injury. It is found that the compound can rapidly target ischemia-reperfusion damaged myocardial cells, inhibit ROS / MDA oxidative stress, quench inflammation storm, and reversely change mitochondrial membrane potential collapse, down-regulate pro-apoptotic protein Bax and up-regulate anti-apoptotic protein Bcl-2, and then inhibit Caspase 3 cleavage, thereby effectively blocking a lethal apoptosis network of myocardial cells from the source. The drug can significantly improve the survival rate of myocardial cells and reduce the myocardial infarction area, and provides a multi-target, mechanism clear new candidate drug for clinical prevention and treatment of acute cardiovascular critical illness.

The application discloses application of vidarabine phosphate in preparation of a medicine for treating liver ischemia-reperfusion injury, and relates to the field of biological medicines. The application finds that vidarabine phosphate can obviously reduce serum liver enzyme levels, obviously reduce GZMB accumulation in liver tissues and expression of inflammation-related factors including Il-1beta, Tnf-alpha and Mmp9, indicates that liver inflammation reaction is reduced, and reduces liver cell apoptosis-related protein cleaved-caspase 3 levels and liver histological injury. In summary, the application first finds application of vidarabine phosphate in treating liver ischemia-reperfusion injury, which can play a role in improving liver enzyme levels and reducing liver inflammatory injury, and has wide clinical application value.

A method is provided to increase the expression of the genes CASP3 and THBD; and decrease the expression of the genes COL18A1, CPB2, NPR1, OCLN, BMP2, CLCL6, IL12B, SELPLG, CX3CL1, CASP3, THBD, COL18A1, CPB2, NPR1, CLDN5, CLD3, PIGF, BDNF, CNTF, VEGF-A, CAM-1, PGF, FOX-01, FOX-04, PDGFB, TGFA, HGF, VE-Cadherin, or PLAU. As a result, conditions associated with expression of these genes are treated. Caspase 3 is encoded by CASP3 (GenBank assembly accession: GCA_000001405.22) and cleaves and activates caspases 6 and 7; and the protein itself is processed and activated by caspases 8, 9, and 10. Caspase 3 is the predominant caspase involved in the cleavage of amyloid-beta 4A precursor protein, which is associated with neuronal death in Alzheimer's disease and after spinal cord injury. As caspase 3 is implicated in apoptosis upregulation of CASP3 can be used to induce dysfunction cell removal.

The application discloses application of 1-aminocyclopropane carboxylic acid in preparation of a glioma treatment drug. The 1-aminocyclopropane carboxylic acid of the application not only significantly inhibits the expression level of glial fibrillary acidic protein of glioma cells, but also effectively inhibits the expression and phosphorylation modification of extracellular signal-regulated kinase 1 / 2 and protein kinase B, blocks the cell proliferation signal mediated by the MAPK / ERK and PI3K / Akt / mTOR signal pathways, and activates the cell apoptosis signal mediated by caspase 3, so that the proliferation of glioma cells is inhibited, the growth speed of a xenograft of a nude mouse is effectively slowed down, the volume and mass of tumor tissues are significantly reduced, and a significant therapeutic effect is achieved.